August 29, 2016
Three-dimensional images from cardiovascular magnetic resonance (CMR) scans detected carotid artery thickening -- an early signal of cardiovascular disease -- in a higher proportion of HIV patients with low traditional cardiovascular risk than in an HIV-negative comparison group, according to a recent study. This difference between HIV-positive cases and HIV-negative controls proved greater in women than men in this 68-person comparison.
Carotid artery intima-media thickness (cIMT) predicts cardiovascular disease in HIV-negative populations. But cIMT results in HIV patients have proved inconsistent, probably because of differences in study design and ultrasound methodology. Because CMR offers several advantages over ultrasound, including a three-dimensional image, a London team conducted this case-control comparison.
In a study published in the April 15 issue of JAIDS, researchers recruited 33 adults who had HIV infection for at least two years, were taking a stable antiretroviral regimen and had a viral load below 50 copies/mL. They excluded people with past or current cardiovascular disease, a family history of premature vascular disease or major modifiable risk factors including smoking, hypertension, hyperlipidemia and diabetes. Participants could not have a Framingham cardiovascular risk score above 10%. A 35-person historical control group matched to cases by age and sex had similarly low cardiovascular risk.
The 33 people with HIV and the 35 controls were similar in age (mean 45.2 and 46.9 years) and in proportion of men (57% and 55%). The HIV group included a lower proportion of whites (48% versus 85%) and a higher proportion of blacks (42% versus 5%). The groups did not differ significantly in blood pressure, total cholesterol or 10-year Framingham cardiovascular risk (mean 3.97% and 3.72%). The HIV group had taken antiretrovirals for an average of 7.5 years and had an average CD4 count of 638 cells/mm3.
Carotid wall thickness as indicated by W/OW ratio proved significantly greater in people with than without HIV infection (average 36.7% versus 32.5%, P < .0001). The difference between people with and without HIV was larger in women (36.4% versus 31.3%, P = .0002) than in men (36.2% versus 33.4%, P = .0019). Participants with and without HIV did not differ significantly in total lumen volume, total wall volume, total vessel volume or distensibility. W/OW ratio, total wall volume and total vessel volume increased with age in participants with and without HIV. Carotid CMR detected no plaques in either group.
Multivariate analysis identified a significant association between W/OW ratio and HIV status, independent of age (r = 4.37, P = .001).
Because the HIV group had thicker artery walls than HIV-negative controls in this study of people with very low traditional cardiovascular risk, the researchers suggest that "the rate of vascular events is likely to remain elevated in HIV-patients despite aggressive treatment of cardiovascular risk factors, highlighting the need for improved patient and health care provider education to detect and manage aggressively early signs of cardiovascular disease." And because everyone with HIV in this study had a viral load below 50 copies/mL, the authors believe heightened cardiovascular risk with HIV "does not seem to be abolished by viral suppression," perhaps because of ongoing low-grade inflammation and T-cell activation. The researchers suggest that the greater between-group difference in wall thickening seen in women than men may mean HIV "may cause excess atherosclerosis in HIV-infected females through changes in [cardioprotective] sex hormones relative to controls."
Mark Mascolini writes about HIV infection.
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